{{Short description|Cognitive process}} {{distinguish|Salience (neuroscience)}} {{Use dmy dates|date=March 2017}} '''Motivational salience''' is a cognitive process and a form of attention that ''motivates'' or propels an individual's behavior towards or away from a particular object, perceived event or outcome.<ref name="Motivational salience">{{cite journal | vauthors = Puglisi-Allegra S, Ventura R | title = Prefrontal/accumbal catecholamine system processes high motivational salience | journal = Front. Behav. Neurosci. | volume = 6 | pages = 31 | date = June 2012 | pmid = 22754514 | pmc = 3384081 | doi = 10.3389/fnbeh.2012.00031 | quote = Motivational salience regulates the strength of goal seeking, the amount of risk taken and the energy invested from mild to extreme. ... Motivation can be conceptually described as a continuum along which stimuli can either reinforce or punish responses to other stimuli. Behaviorally, stimuli that reinforce are called rewarding and those that punish aversive (Skinner, 1953). Reward and aversion describe the impact a stimulus has on behavior, and provided of motivational properties, thus able to induce attribution of motivational salience. ... Attribution of motivational salience is related to the salience of an UCS (Dallman et al., 2003; Pecina et al., 2006). Thus, the more salient an UCS the more likely a neutral (to-be-conditioned) stimulus will be associated with it through motivational salience attribution. Prior experience is a major determinant of the motivational impact of any given stimulus (Borsook et al., 2007) and emotional arousal induced by motivational stimuli increases the attention given to stimuli influencing both the initial perceptual encoding and the consolidation process (Anderson et al., 2006; McGaugh, 2006).| doi-access = free }}</ref> Motivational salience regulates the intensity of behaviors that facilitate the attainment of a particular goal, the amount of time and energy that an individual is willing to expend to attain a particular goal, and the amount of risk that an individual is willing to accept while working to attain a particular goal.<ref name="Motivational salience" />
Motivational salience is composed of two component processes that are defined by their attractive or aversive effects on an individual's behavior relative to a particular stimulus: ''incentive salience'' and ''aversive salience''.<ref name="Motivational salience" /> '''Incentive salience''' is the attractive form of motivational salience that causes approach behavior, and is associated with operant reinforcement, desirable outcomes, and pleasurable stimuli.<ref name="NAcc function" /><ref name=Schultz/> '''Aversive salience''' (sometimes known as fearful salience<ref>{{cite book |last1=Berridge |first1=Kent |author1-link=Kent C. Berridge |editor1-last=Gruber |editor1-first=June |title=The Oxford Handbook of Positive Emotion and Psychopathology |date=2019 |publisher=Oxford University Press |location=Oxford/New York |page=184 |chapter=12: A Liking Versus Wanting Perspective on Emotion and the Brain}}</ref>) is the aversive form of motivational salience that causes avoidance behavior, and is associated with operant punishment, undesirable outcomes, and unpleasant stimuli.<ref name="Aversive salience">{{cite book|author1=Koob GF, Moal ML|title=Neurobiology of Addiction|date=2006|publisher=Elsevier/Academic Press|location=Amsterdam|isbn=9780080497372|page=415|url=https://books.google.com/books?id=Sjn6I6QMxdwC&q=aversive+salience&pg=PA415}}</ref>
==Incentive salience== {{addiction glossary}} '''Incentive salience''' is a cognitive process that grants a "desire" or "want" attribute, which includes a motivational component to a rewarding stimulus.<ref name="Motivational salience" /><ref name="NAcc function" /><ref name=Schultz /><ref name="Incentive salience and motivation review" /> ''Reward'' is the attractive and motivational property of a stimulus that induces appetitive behavior – also known as approach behavior – and consummatory behavior.<ref name=Schultz>{{cite journal | vauthors = Schultz W | year = 2015 | title = Neuronal reward and decision signals: from theories to data | journal = Physiological Reviews | volume = 95 | issue = 3 | pages = 853–951 | pmid = 26109341 | pmc = 4491543 | doi=10.1152/physrev.00023.2014 | quote = Rewards in operant conditioning are positive reinforcers. ... Operant behavior gives a good definition for rewards. Anything that makes an individual come back for more is a positive reinforcer and therefore a reward. Although it provides a good definition, positive reinforcement is only one of several reward functions. ... Rewards are attractive. They are motivating and make us exert an effort. ... Rewards induce approach behavior, also called appetitive or preparatory behavior, and consummatory behavior. ... Thus any stimulus, object, event, activity, or situation that has the potential to make us approach and consume it is by definition a reward. ... Rewarding stimuli, objects, events, situations, and activities consist of several major components. First, rewards have basic sensory components (visual, auditory, somatosensory, gustatory, and olfactory) ... Second, rewards are salient and thus elicit attention, which are manifested as orienting responses (FIGURE 1, middle). The salience of rewards derives from three principal factors, namely, their physical intensity and impact (physical salience), their novelty and surprise (novelty/surprise salience), and their general motivational impact shared with punishers (motivational salience). A separate form not included in this scheme, incentive salience, primarily addresses dopamine function in addiction and refers only to approach behavior (as opposed to learning) ... Third, rewards have a value component that determines the positively motivating effects of rewards and is not contained in, nor explained by, the sensory and attentional components (FIGURE 1, right). This component reflects behavioral preferences and thus is subjective and only partially determined by physical parameters. Only this component constitutes what we understand as a reward. It mediates the specific behavioral reinforcing, approach generating, and emotional effects of rewards that are crucial for the organism's survival and reproduction, whereas all other components are only supportive of these functions. ... These emotions are also called liking (for pleasure) and wanting (for desire) in addiction research (471) and strongly support the learning and approach generating functions of reward.}}</ref> The "wanting" of incentive salience differs from "liking" in the sense that liking is the pleasure that is immediately gained from the acquisition or consumption of a rewarding stimulus;<ref name="Incentive salience and motivation review" /><ref name="Pleasure system - incentive sensitization" /> the "wanting" of incentive salience serves a "motivational magnet" quality of a rewarding stimulus that makes it a desirable and attractive goal, transforming it from a mere sensory experience into something that commands attention, induces approach, and causes it to be sought out.<ref name="Incentive salience and motivation review">{{cite journal | vauthors = Berridge KC | title = From prediction error to incentive salience: mesolimbic computation of reward motivation | journal = Eur. J. Neurosci. | volume = 35 | issue = 7 | pages = 1124–1143 | date = April 2012 | pmid = 22487042 | pmc = 3325516 | doi = 10.1111/j.1460-9568.2012.07990.x | quote = Here I discuss how mesocorticolimbic mechanisms generate the motivation component of incentive salience. Incentive salience takes Pavlovian learning and memory as one input and as an equally important input takes neurobiological state factors (e.g. drug states, appetite states, satiety states) that can vary independently of learning. Neurobiological state changes can produce unlearned fluctuations or even reversals in the ability of a previously learned reward cue to trigger motivation. Such fluctuations in cue-triggered motivation can dramatically depart from all previously learned values about the associated reward outcome. ... Associative learning and prediction are important contributors to motivation for rewards. Learning gives incentive value to arbitrary cues such as a Pavlovian conditioned stimulus (CS) that is associated with a reward (unconditioned stimulus or UCS). Learned cues for reward are often potent triggers of desires. For example, learned cues can trigger normal appetites in everyone, and can sometimes trigger compulsive urges and relapse in addicts. ... A brief CS encounter (or brief UCS encounter) often primes a pulse of elevated motivation to obtain and consume more reward UCS. This is a signature feature of incentive salience. ... When a Pavlovian CS+ is attributed with incentive salience it not only triggers 'wanting’ for its UCS, but often the cue itself becomes highly attractive – even to an irrational degree. This cue attraction is another signature feature of incentive salience. ... An attractive CS often elicits behavioral motivated approach, and sometimes an individual may even attempt to 'consume’ the CS somewhat as its UCS (e.g., eat, drink, smoke, have sex with, take as drug). 'Wanting’ of a CS can turn also turn the formerly neutral stimulus into an instrumental conditioned reinforcer, so that an individual will work to obtain the cue (however, there exist alternative psychological mechanisms for conditioned reinforcement too). ... Two recognizable features of incentive salience are often visible that can be used in neuroscience experiments: (i) UCS-directed 'wanting' – CS-triggered pulses of intensified 'wanting' for the UCS reward; and (ii) CS-directed 'wanting' – motivated attraction to the Pavlovian cue, which makes the arbitrary CS stimulus into a motivational magnet.}}</ref><ref name="Pleasure system - incentive sensitization" />
Incentive salience is regulated by a number of brain structures, but it is assigned to stimuli by a region of the ventral striatum known as the nucleus accumbens shell.<ref name="Motivational salience" /><ref name="NAcc function">{{cite book |vauthors=Malenka RC, Nestler EJ, Hyman SE |veditors=Sydor A, Brown RY | title = Molecular Neuropharmacology: A Foundation for Clinical Neuroscience | year = 2009 | publisher = McGraw-Hill Medical | location = New York | isbn = 978-0-07-148127-4 | pages = 147–148, 367, 376 | edition = 2nd | quote= VTA DA neurons play a critical role in motivation, reward-related behavior (Chapter 15), attention, and multiple forms of memory. This organization of the DA system, wide projection from a limited number of cell bodies, permits coordinated responses to potent new rewards. Thus, acting in diverse terminal fields, dopamine confers motivational salience (“wanting”) on the reward itself or associated cues (nucleus accumbens shell region), updates the value placed on different goals in light of this new experience (orbital prefrontal cortex), helps consolidate multiple forms of memory (amygdala and hippocampus), and encodes new motor programs that will facilitate obtaining this reward in the future (nucleus accumbens core region and dorsal striatum). In this example, dopamine modulates the processing of sensorimotor information in diverse neural circuits to maximize the ability of the organism to obtain future rewards. ...<br />The brain reward circuitry that is targeted by addictive drugs normally mediates the pleasure and strengthening of behaviors associated with natural reinforcers, such as food, water, and sexual contact. Dopamine neurons in the VTA are activated by food and water, and dopamine release in the NAc is stimulated by the presence of natural reinforcers, such as food, water, or a sexual partner. ...<br />The NAc and VTA are central components of the circuitry underlying reward and memory of reward. As previously mentioned, the activity of dopaminergic neurons in the VTA appears to be linked to reward prediction. The NAc is involved in learning associated with reinforcement and the modulation of motoric responses to stimuli that satisfy internal homeostatic needs. The shell of the NAc appears to be particularly important to initial drug actions within reward circuitry; addictive drugs appear to have a greater effect on dopamine release in the shell than in the core of the NAc.}}</ref><ref name="Incentive salience and motivation review" /> Incentive salience is primarily regulated by dopamine neurotransmission in the mesocorticolimbic projection,{{#tag:ref|The mesocorticolimbic projection is a group of dopamine pathways that connects the ventral tegmental area to the nucleus accumbens and prefrontal cortex.|group="note"}} but activity in other dopaminergic pathways and hedonic hotspots (e.g., the ventral pallidum) also modulate incentive salience.<ref name="NAcc function" /><ref name="Incentive salience and motivation review" /><ref name="Pleasure system - incentive sensitization">{{cite journal | vauthors = Berridge KC, Kringelbach ML | title = Pleasure systems in the brain | journal = Neuron | volume = 86 | issue = 3 | pages = 646–664 | date = May 2015 | pmid = 25950633 | doi = 10.1016/j.neuron.2015.02.018 | quote = An important goal in future for addiction neuroscience is to understand how intense motivation becomes narrowly focused on a particular target. Addiction has been suggested to be partly due to excessive incentive salience produced by sensitized or hyper-reactive dopamine systems that produce intense 'wanting’ (Robinson and Berridge, 1993). But why one target becomes more 'wanted’ than all others has not been fully explained. In addicts or agonist-stimulated patients, the repetition of dopamine-stimulation of incentive salience becomes attributed to particular individualized pursuits, such as taking the addictive drug or the particular compulsions. In Pavlovian reward situations, some cues for reward become more 'wanted’ more than others as powerful motivational magnets, in ways that differ across individuals (Robinson et al., 2014b; Saunders and Robinson, 2013). ... However, hedonic effects might well change over time. As a drug was taken repeatedly, mesolimbic dopaminergic sensitization could consequently occur in susceptible individuals to amplify 'wanting’ (Leyton and Vezina, 2013; Lodge and Grace, 2011; Wolf and Ferrario, 2010), even if opioid hedonic mechanisms underwent down-regulation due to continual drug stimulation, producing 'liking’ tolerance. Incentive-sensitization would produce addiction, by selectively magnifying cue-triggered 'wanting’ to take the drug again, and so powerfully cause motivation even if the drug became less pleasant (Robinson and Berridge, 1993).| pmc=4425246}}</ref><ref>{{Cite book|title = Chapter 18 – From Experienced Utility to Decision Utility|doi=10.1016/B978-0-12-416008-8.00018-8|publisher = Academic Press|date = 1 January 2014|location = San Diego|isbn = 978-0-12-416008-8|pages = 335–351|first1 = Kent C.|last1 = Berridge|first2 = John P.|last2 = O’Doherty|editor-first = Paul W. GlimcherErnst|editor-last = Fehr}}</ref>
== Aversive salience == '''Aversive salience''' describes the motivation behind avoidance behavior towards a negative presenting stimulus developed through learning and memory recall.<ref name=":1">{{Cite journal |last=Ghazizadeh |first=Ali |last2=Hikosaka |first2=Okihide |date=2022-10-25 |title=Salience memories formed by value, novelty and aversiveness jointly shape object responses in the prefrontal cortex and basal ganglia |url=https://www.nature.com/articles/s41467-022-33514-3 |journal=Nature Communications |language=en |volume=13 |issue=1 |pages=6338 |doi=10.1038/s41467-022-33514-3 |issn=2041-1723|pmc=9596424 }}</ref> Avoidance behavior emerges when a once novel stimulus becomes associated to an undesirable outcome. In Pavlovian conditioning, developed by Ivan Pavlov, pairing of a neutral conditioned stimulus (such as a soft tone) with an aversive unconditioned stimulus (such as bitter flavors, loud tones, electric shocks) results in association of the once neutral stimulus with a negative outcome. The previously neutral stimulus elicits avoidance behavior upon future presentation.<ref>{{Cite journal |last=Sengupta |first=Auntora |last2=Yau |first2=Joanna O. Y. |last3=Jean-Richard-Dit-Bressel |first3=Philip |last4=Liu |first4=Yu |last5=Millan |first5=E. Zayra |last6=Power |first6=John M. |last7=McNally |first7=Gavan P. |date=2018-03-21 |title=Basolateral Amygdala Neurons Maintain Aversive Emotional Salience |url=https://www.jneurosci.org/content/38/12/3001 |journal=Journal of Neuroscience |language=en |volume=38 |issue=12 |pages=3001–3012 |doi=10.1523/JNEUROSCI.2460-17.2017 |issn=0270-6474 |pmid=29079689|pmc=6596078 }}</ref>
'''Neural Responses in Formation of Aversive Salience'''
Neural circuity between areas of the prefrontal cortex and basal ganglia encode aversive salience based on behavioral relevance rather than mere negative valance of the stimulus.<ref name=":1" /> Neural recognition of behavioral importance of aversive stimuli promote '''adaptive avoidance''' and drive goal '''motivated behavior'''.
Aversive salience can be influenced by distinctive changes in neural firing. Silencing of specific neural populations within the parabrachial nucleus reduces acquisition of conditioned taste aversion (CTA).<ref>{{Cite journal |last=Carter |first=Matthew E. |last2=Han |first2=Sung |last3=Palmiter |first3=Richard D. |date=2015-03-18 |title=Parabrachial calcitonin gene-related peptide neurons mediate conditioned taste aversion |url=https://pubmed.ncbi.nlm.nih.gov/25788675 |journal=The Journal of Neuroscience|volume=35 |issue=11 |pages=4582–4586 |doi=10.1523/JNEUROSCI.3729-14.2015 |issn=1529-2401 |pmc=4363386 |pmid=25788675}}</ref> Activation of distinct neural populations within the parabrachial nucleus can establish CTA.<ref>{{Cite journal |last=Chen |first=Jane Y. |last2=Campos |first2=Carlos A. |last3=Jarvie |first3=Brooke C. |last4=Palmiter |first4=Richard D. |date=2018-11-21 |title=Parabrachial CGRP Neurons Establish and Sustain Aversive Taste Memories |url=https://www.cell.com/neuron/abstract/S0896-6273(18)30834-1 |journal=Neuron |language=English |volume=100 |issue=4 |pages=891–899.e5 |doi=10.1016/j.neuron.2018.09.032 |issn=0896-6273 |pmid=30344042}}</ref>
==Clinical significance== {{Further|Pavlovian instrumental transfer#Clinical significance}}
===Addiction=== {{Further|Addiction#Reward sensitization}} The assignment of incentive salience to stimuli is dysregulated in addiction.<ref name="Motivational salience" /><ref name="Incentive salience and motivation review" /><ref name="Pleasure system - incentive sensitization" /><ref name="Reinforcement in addiction" /> Addictive drugs are intrinsically rewarding (not to be confused with pleasure) and therefore function as primary positive reinforcers of continued drug use that are assigned incentive salience.<ref name="Schultz" /><ref name="Incentive salience and motivation review" /><ref name="Pleasure system - incentive sensitization"/><ref name="Reinforcement in addiction">{{cite book | vauthors = Edwards S | title = Neuroscience for Addiction Medicine: From Prevention to Rehabilitation - Constructs and Drugs | chapter = Reinforcement principles for addiction medicine; from recreational drug use to psychiatric disorder | journal = Prog. Brain Res. | volume = 223 | pages = 63–76 | year = 2016 | pmid = 26806771 | doi = 10.1016/bs.pbr.2015.07.005 | quote = Abused substances (ranging from alcohol to psychostimulants) are initially ingested at regular occasions according to their positive reinforcing properties. Importantly, repeated exposure to rewarding substances sets off a chain of secondary reinforcing events, whereby cues and contexts associated with drug use may themselves become reinforcing and thereby contribute to the continued use and possible abuse of the substance(s) of choice. ...<br />An important dimension of reinforcement highly relevant to the addiction process (and particularly relapse) is secondary reinforcement (Stewart, 1992). Secondary reinforcers (in many cases also considered conditioned reinforcers) likely drive the majority of reinforcement processes in humans. In the specific case of drug [addiction], cues and contexts that are intimately and repeatedly associated with drug use will often themselves become reinforcing ... A fundamental piece of Robinson and Berridge's incentive-sensitization theory of addiction posits that the incentive value or attractive nature of such secondary reinforcement processes, in addition to the primary reinforcers themselves, may persist and even become sensitized over time in league with the development of drug addiction (Robinson and Berridge, 1993). ...<br />Negative reinforcement is a special condition associated with a strengthening of behavioral responses that terminate some ongoing (presumably aversive) stimulus. In this case we can define a negative reinforcer as a motivational stimulus that strengthens such an “escape” response. Historically, in relation to drug addiction, this phenomenon has been consistently observed in humans whereby drugs of abuse are self-administered to quench a motivational need in the state of withdrawal (Wikler, 1952).| series = Progress in Brain Research | isbn = 9780444635457 }}</ref> During the development of an addiction, the repeated association of otherwise neutral and even non-rewarding stimuli with drug consumption triggers an associative learning process that causes these previously neutral stimuli to act as conditioned positive reinforcers of addictive drug use (i.e., these stimuli start to function as drug cues).<ref name="Incentive salience and motivation review" /><ref name="Pleasure system - incentive sensitization" /><ref name="Reinforcement in addiction" /> As conditioned positive reinforcers of drug use, these previously neutral stimuli are assigned incentive salience (which manifests as a craving) – sometimes at pathologically high levels due to reward sensitization – which can transfer to the primary reinforcer (e.g., the use of an addictive drug) with which it was originally paired.<ref name="Incentive salience and motivation review" /><ref name="Pleasure system - incentive sensitization" /><ref name="Reinforcement in addiction" /> Thus, if an individual remains abstinent from drug use for some time and encounters one of these drug cues, a craving for the associated drug may reappear. For example, anti-drug agencies previously used posters with images of drug paraphernalia as an attempt to show the dangers of drug use. However, such posters are no longer used because of the effects of incentive salience in causing relapse upon sight of the stimuli illustrated in the posters.{{citation needed|date=May 2018}}
In addiction, the "liking" (pleasure or hedonic value) of a drug or other stimulus becomes dissociated from "wanting" (i.e., desire or craving) due to the sensitization of incentive salience.<ref>Berridge, K.C., Robinson, T.E. What is the role of dopamine in reward: hedonic impact, reward learning, or incentive salience? Brain Res Brain Res Rev. 1998 Dec; 28(3):309–69.</ref> In fact, if the incentive salience associated with drug-taking becomes pathologically amplified, the user may want the drug more and more while liking it less and less as tolerance develops to the drug's pleasurable effects.<ref name="Pleasure system - incentive sensitization" />
==Neuropsychopharmacology==
===Dopaminergic psychostimulants=== Amphetamine improves task saliency (motivation to perform a task) and increases arousal (wakefulness), in turn promoting goal-directed behavior.<ref name="Malenka_2009" /><ref name="Malenka NAcc">{{cite book |vauthors=Malenka RC, Nestler EJ, Hyman SE |veditors=Sydor A, Brown RY | title = Molecular Neuropharmacology: A Foundation for Clinical Neuroscience | year = 2009 | publisher = McGraw-Hill Medical | location = New York, USA | isbn = 9780071481274 | page = 266 | edition = 2nd | chapter = Chapter 10: Neural and Neuroendocrine Control of the Internal Milieu | quote = Dopamine acts in the nucleus accumbens to attach motivational significance to stimuli associated with reward.}}</ref><ref name="Continuum">{{cite journal |vauthors=Wood S, Sage JR, Shuman T, Anagnostaras SG |title=Psychostimulants and cognition: a continuum of behavioral and cognitive activation |journal=Pharmacol. Rev. |volume=66 |issue=1 |pages=193–221 |date=January 2014 |pmid=24344115 |pmc=3880463 |doi=10.1124/pr.112.007054}}</ref> The reinforcing and motivational salience-promoting effects of amphetamine are mostly due to enhanced dopaminergic activity in the mesolimbic pathway.<ref name="Malenka_2009">{{cite book|vauthors=Malenka RC, Nestler EJ, Hyman SE |veditors=Sydor A, Brown RY | title = Molecular Neuropharmacology: A Foundation for Clinical Neuroscience | year = 2009 | publisher = McGraw-Hill Medical | location = New York, USA | isbn = 9780071481274 | pages = 318, 321 | edition = 2nd | chapter = Chapter 13: Higher Cognitive Function and Behavioral Control | quote = Therapeutic (relatively low) doses of psychostimulants, such as methylphenidate and amphetamine, improve performance on working memory tasks both in normal subjects and those with ADHD. ... stimulants act not only on working memory function, but also on general levels of arousal and, within the nucleus accumbens, improve the saliency of tasks. Thus, stimulants improve performance on effortful but tedious tasks ... through indirect stimulation of dopamine and norepinephrine receptors. ...<br />Beyond these general permissive effects, dopamine (acting via D1 receptors) and norepinephrine (acting at several receptors) can, at optimal levels, enhance working memory and aspects of attention.}}</ref>
== Dopaminergic Activity ==
=== Dopamine Response === Distinctive patterns in dopamine activity in response to external stimuli influence ''motivational'' behavior. Tonic dopamine refers to steady dopamine release from dopaminergic neurons at baseline conditions. Phasic dopamine include fast bursts of dopamine activity, represented by spikes in activation or inhibition from tonic levels, upon presentation of an external stimulus. External stimuli can include aversive and appetitive cues both eliciting distinct dopaminergic response patterns.<ref>{{Cite journal|title=Neuroimaging of the dopamine/reward system in adolescent drug use|url=https://www.cambridge.org/core/journals/cns-spectrums/article/abs/neuroimaging-of-the-dopaminereward-system-in-adolescent-drug-use/98C274F37C34CEB6E39CF979F10E02C9|journal=CNS Spectrums|date=22 June 2015|issn=1092-8529|pages=427–441|volume=20|issue=4|doi=10.1017/S1092852915000395|language=en|first=Monique|last=Ernst|first2=Monica|last2=Luciana|pmc=4560964}}</ref> Neural populations which activate to distinct cues show uniformity in activity pattern upon presentation of similar cues, such the same population of neurons that respond to an aversive cue respond similarly to another aversive cue.<ref>{{Cite journal|title=A Neural Substrate of Prediction and Reward|url=https://www.science.org/doi/10.1126/science.275.5306.1593|journal=Science|date=1997-03-14|pages=1593–1599|volume=275|issue=5306|doi=10.1126/science.275.5306.1593|first=Wolfram|last=Schultz|first2=Peter|last2=Dayan|first3=P. Read|last3=Montague|url-access=subscription}}</ref>
Increased phasic dopaminergic activity influences '''motivational salience'''. An appetitive predicting stimulus and reward acquisition elicit the same patterns of activity.<ref name=":0">{{Cite journal |last=Schultz |first=Wolfram |date=1 December 2000 |title=Multiple reward signals in the brain |url=https://www.nature.com/articles/35044563 |journal=Nature Reviews Neuroscience |language=en |volume=1 |issue=3 |pages=199–207 |doi=10.1038/35044563 |issn=1471-0048|url-access=subscription }}</ref> Suggesting reward predicting cues gain '''incentive salience.''' During an aversive stimulus, phasic increased dopaminergic firing is minimal, with a greater response in phasic inhibition and majority of neurons unresponsive.<ref>{{Cite journal |last=Guarraci |first=Fay A. |last2=Kapp |first2=Bruce S. |date=1999-03-01 |title=An electrophysiological characterization of ventral tegmental area dopaminergic neurons during differential pavlovian fear conditioning in the awake rabbit |url=https://www.sciencedirect.com/science/article/pii/S0166432898001028 |journal=Behavioural Brain Research |volume=99 |issue=2 |pages=169–179 |doi=10.1016/S0166-4328(98)00102-8 |issn=0166-4328|url-access=subscription }}</ref> Suppressing dopamine effects through neuroleptics or lesions to areas in the dopamine pathway, suppressed motivational behavior seen through decreased participation to rewarding tasks.<ref>{{Cite journal |last=Wise |first=Roy A. |date=1 June 2004 |title=Dopamine, learning and motivation |url=https://www.nature.com/articles/nrn1406 |journal=Nature Reviews Neuroscience |language=en |volume=5 |issue=6 |pages=483–494 |doi=10.1038/nrn1406 |issn=1471-0048|url-access=subscription }}</ref>
'''Reward Prediction Error Hypothesis''' thumb|368x368px|Illustration of the Reward Prediction Error Hypothesis. Dopaminergic firing patterns in response to rewards and reward-predicting cues. The "Reward Prediction Error Hypothesis" developed by Neuroscientist Wolfram Schultz, associates dopamine response to reward expectation.<ref name=":0" /> Schultz describes phasic timing of dopamine activity as a indication of reward processing, using aspects of the reward system establishing the mechanisms of learning.
Novel tasks elicit positive spikes in phasic dopamine. The same positive spikes are elicited during reward acquisition.<ref name=":0" /> As associations between the reward-predicting cue and the reward develop during learning, phasic dopamine activity shifts from firing at reward acquisition to upon presentation of the cue. This shift in firing is described as associative learning by the 'Reward Prediction Error Hypothesis' as the reward has become expected. When the expected reward is removed, phasic dopamine shows large inhibition represented by a dip in activity.<ref name=":0" /> The combination between acquisition of the reward being "better than expected" and absence of the reward being "worse than expected" is what the Hypothesis describes as "reinforcement learning". Predicting future rewards drives behavioral outcomes and serve as a neural rendering to motivation.
==See also== {{col-list| * Dalbir Bindra * Conditioned place preference * Desire * Dopamine * Kent C. Berridge * {{Section link|Medium spiny neuron|Ventral striatal MSNs}} * Pavlovian-instrumental transfer * Pleasure * Reward system }}
==Notes== {{Reflist|group=note}}
==References== {{reflist|30em}}
{{Addiction|state=expanded}}
Category:Addiction Category:Amphetamine Category:Attention Category:Behaviorism Category:Behavior modification Category:Cognition Category:Cognitive psychology Category:Motivation Category:Neuropsychology